For the entire Vanderbilt validation set (n=170, 54% malignant), the AUC was 0.87 (95% CI 0.81-0.92) for the Brock model and 0.90 (95% CI 0.85-0.94) for the BRODERS model. Using the optimal cut-off determined by Youden's index, the sensitivity was 92.3%, the specificity was 62.0%, the positive (PPV) and negative predictive values (NPV) were 73.7% and 87.5%, respectively. For nodules with intermediate pre-test probability of malignancy, Brock score of 5-65% (n=97), the sensitivity and specificity were 94% and 46%, respectively, the PPV was 78.4% and the NPV was 79.2%. The BRODERS radiomic predictive model performs well on an independent dataset and may facilitate the management of indeterminate pulmonary nodules. The BRODERS radiomic predictive model performs well on an independent dataset and may facilitate the management of indeterminate pulmonary nodules. Bronchopulmonary dysplasia (BPD) is a common complication of preterm birth. Lung function and imaging are classically used to assess BPD. Functional Respiratory Imaging (FRI) combines a structural and functional assessment of the airways and their vasculature. We aimed to assess BPD with FRI and to correlate these findings with the clinical presentation. We included 37 adolescents with a history of preterm birth (22 BPD cases and 15 preterm controls). The study protocol included a detailed history, lung function testing and CT (at TLC and FRC) with FRI. CT images were also assessed using the Aukland scoring system. BPD patients had lower FEV /FVC (p=0.02) and impaired diffusion capacity (p=0.02).Aukland CT scores were not different between the two groups. FRI analysis showed higher lobar volumes in BPD patients at FRC (p<0.01) but not at TLC. Airway resistance was significantly higher in the BPD group, especially in the distal airways. Additionally, FRI showed more air trapping in BPD patients, in co better understand the long-term sequelae of BPD.Bronchiolitis obliterans syndrome (BOS) is a major complication after lung transplantation (LTx). BOS is characterised by massive peribronchial fibrosis, leading to air trapping induced pulmonary dysfunction. Cathepsin B, a lysosomal cysteine-protease, was shown to enforce fibrotic pathways in several diseases. However, the relevance of Cathepsin B in BOS progression has not yet been addressed. The aim of the study was to elucidate the function of Cathepsin B in BOS pathogenesis.We determined Cathepsin B levels in BAL fluid and lung tissue from healthy donors (HD) and BOS LTx patients. Furthermore, Cathepsin B activity was assessed via a FRET-based assay and protein expression was determined using Western blotting, ELISA, and immunostaining. To investigate the impact of Cathepsin B in the pathophysiology of BOS, we used an in-vivo orthotopic left-LTx mouse model. Mechanistic studies were performed in-vitro using macrophage and fibroblast cell lines.We found a significant increase of Cathepsin B activity in BALF and lung tissue from BOS patients, as well as in our murine model of lymphocytic bronchiolitis (LB). Moreover, Cathepsin B activity was associated with an increased biosynthesis of collagen, and negatively affected lung function. Interestingly, we observed that Cathepsin B was mainly expressed in macrophages that infiltrated areas characterised by a massive accumulation of collagen deposition. Mechanistically, macrophage-derived Cathepsin B contributed to TGF-β1-dependent activation of fibroblasts, and its inhibition reversed the phenotype.Infiltrating macrophages release active Cathepsin B promoting fibroblast-activation and subsequent collagen deposition, driving BOS. Cathepsin B represents a promising therapeutic target to prevent the progression of BOS. Elevated levels of IL-17A were detected in the airways of patients with cystic fibrosis (CF), but its cellular sources and role in the pathogenesis of CF lung disease remain poorly understood. The aim of this study was to determine the sources of IL-17A and its role in airway inflammation and lung damage in CF. We performed flow cytometry to identify IL-17A-producing cells in lungs and peripheral blood from CF patients and β-epithelial Na channel transgenic ( -Tg) mice with CF-like lung disease and determined effects of genetic deletion of and on the pulmonary phenotype of -Tg mice. T helper (Th)17 cells, CD3 CD8 , γδ T cells, invariant natural killer T cells (iNKT) and innate lymphoid cells (ILCs) contribute to IL-17A secretion in lung tissue, lymph nodes and peripheral blood of patients with CF. -Tg mice displayed increased pulmonary expression of and elevated IL-17A-producing innate and adaptive lymphocytes with a major contribution by γδ T cells. Lack of IL-17A, but not RAG1 reduced neutrophilic airway inflammation in -Tg mice. Genetic deletion of or had no effect on mucus obstruction, but reduced structural lung damage and revealed an IL-17A-dependent macrophage activation in -Tg mice. We identify innate and adaptive sources of IL-17A in CF lung disease. Our data demonstrate that IL-17A contributes to airway neutrophilia, macrophage activation and structural lung damage in CF-like lung disease in mice. These results suggest IL-17A as a novel target for anti-inflammatory therapy of CF lung disease. We identify innate and adaptive sources of IL-17A in CF lung disease. https://www.selleckchem.com/products/cc-930.html Our data demonstrate that IL-17A contributes to airway neutrophilia, macrophage activation and structural lung damage in CF-like lung disease in mice. These results suggest IL-17A as a novel target for anti-inflammatory therapy of CF lung disease. Current guidelines suggest treating cancer patients with incidental pulmonary embolism (PE) similar to those with clinically-suspected and confirmed PE. However, the natural history of these presentations has not been thoroughly compared. We used the data from the RIETE registry to compare the 3-month outcomes in patients with active cancer and incidental PE those with clinically-suspected and confirmed PE. The primary outcome was 90-day all-cause mortality. Secondary outcomes were PE-related mortality, symptomatic PE recurrences and major bleeding. From July 2012 to January 2019, 946 cancer patients with incidental asymptomatic PE and 2274 with clinically-suspected and confirmed PE were enrolled. Most patients (95% 90%) received low-molecular-weight heparin therapy. During the first 90 days, 598 patients died, including 42 from PE. Patients with incidental PE had a lower all-cause mortality rate than those with suspected and confirmed PE (11% 22%; odds ratio [OR] 0.43; 95%CI 0.34-0.54). Results were consistent for PE-related mortality (0.